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Corticosteroid inhibits IL‐4 signaling through down‐regulation of IL‐4 receptor and STAT6 activity
Author(s) -
So Eui-Young,
Kim Seol-Hee,
Cho Byoung-Soo,
Park Hyun-Hee,
Lee Choong-Eun
Publication year - 2002
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(02)02635-2
Subject(s) - stat6 , tyrosine phosphorylation , signal transduction , receptor , interleukin 4 , biology , cd23 , immune system , chemistry , microbiology and biotechnology , immunoglobulin e , endocrinology , immunology , biochemistry , antibody
Corticosteroids are potent anti‐inflammatory and immunosuppressive agents which down‐regulate cytokine production and action. Yet, contradictory results have been reported for their effects on the interleukin (IL)‐4‐mediated response. Using type II Fc receptor for IgE/CD23 as a target gene, here we report that corticosteroids at 10 −4 –10 −6 M inhibit the IL‐4 signaling pathway in human primary immune cells by down‐regulation of the IL‐4‐induced IL‐4 receptor expression and STAT6 activation. Although functional antagonism between steroid receptor and STAT6 for their transcriptional activity has been recently described, this is the first report that steroid inhibits the IL‐4‐induced STAT6 activity at the level of tyrosine phosphorylation and target DNA binding.